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Gene by stress genome-wide interaction analysis and path analysis identify EBF1 as a cardiovascular and metabolic risk gene.

Publication ,  Journal Article
Singh, A; Babyak, MA; Nolan, DK; Brummett, BH; Jiang, R; Siegler, IC; Kraus, WE; Shah, SH; Williams, RB; Hauser, ER
Published in: Eur J Hum Genet
June 2015

We performed gene-environment interaction genome-wide association analysis (G × E GWAS) to identify SNPs whose effects on metabolic traits are modified by chronic psychosocial stress in the Multi-Ethnic Study of Atherosclerosis (MESA). In Whites, the G × E GWAS for hip circumference identified five SNPs within the Early B-cell Factor 1 (EBF1) gene, all of which were in strong linkage disequilibrium. The gene-by-stress interaction (SNP × STRESS) term P-values were genome-wide significant (Ps = 7.14E-09 to 2.33E-08, uncorrected; Ps = 1.99E-07 to 5.18E-07, corrected for genomic control). The SNP-only (without interaction) model P-values (Ps = 0.011-0.022) were not significant at the conventional genome-wide significance level. Further analysis of related phenotypes identified gene-by-stress interaction effects for waist circumference, body mass index (BMI), fasting glucose, type II diabetes status, and common carotid intimal-medial thickness (CCIMT), supporting a proposed model of gene-by-stress interaction that connects cardiovascular disease (CVD) risk factor endophenotypes such as central obesity and increased blood glucose or diabetes to CVD itself. Structural equation path analysis suggested that the path from chronic psychosocial stress to CCIMT via hip circumference and fasting glucose was larger (estimate = 0.26, P = 0.033, 95% CI = 0.02-0.49) in the EBF1 rs4704963 CT/CC genotypes group than the same path in the TT group (estimate = 0.004, P = 0.34, 95% CI = -0.004-0.012). We replicated the association of the EBF1 SNPs and hip circumference in the Framingham Offspring Cohort (gene-by-stress term P-values = 0.007-0.012) as well as identified similar path relationships. This observed and replicated interaction between psychosocial stress and variation in the EBF1 gene may provide a biological hypothesis for the complex relationship between psychosocial stress, central obesity, diabetes, and cardiovascular disease.

Duke Scholars

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Published In

Eur J Hum Genet

DOI

EISSN

1476-5438

Publication Date

June 2015

Volume

23

Issue

6

Start / End Page

854 / 862

Location

England

Related Subject Headings

  • Trans-Activators
  • Socioeconomic Factors
  • Polymorphism, Single Nucleotide
  • Obesity
  • Metabolic Syndrome
  • Humans
  • Genome-Wide Association Study
  • Genetics & Heredity
  • Gene-Environment Interaction
  • Endophenotypes
 

Citation

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ICMJE
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Singh, A., Babyak, M. A., Nolan, D. K., Brummett, B. H., Jiang, R., Siegler, I. C., … Hauser, E. R. (2015). Gene by stress genome-wide interaction analysis and path analysis identify EBF1 as a cardiovascular and metabolic risk gene. Eur J Hum Genet, 23(6), 854–862. https://doi.org/10.1038/ejhg.2014.189
Singh, Abanish, Michael A. Babyak, Daniel K. Nolan, Beverly H. Brummett, Rong Jiang, Ilene C. Siegler, William E. Kraus, Svati H. Shah, Redford B. Williams, and Elizabeth R. Hauser. “Gene by stress genome-wide interaction analysis and path analysis identify EBF1 as a cardiovascular and metabolic risk gene.Eur J Hum Genet 23, no. 6 (June 2015): 854–62. https://doi.org/10.1038/ejhg.2014.189.
Singh A, Babyak MA, Nolan DK, Brummett BH, Jiang R, Siegler IC, et al. Gene by stress genome-wide interaction analysis and path analysis identify EBF1 as a cardiovascular and metabolic risk gene. Eur J Hum Genet. 2015 Jun;23(6):854–62.
Singh, Abanish, et al. “Gene by stress genome-wide interaction analysis and path analysis identify EBF1 as a cardiovascular and metabolic risk gene.Eur J Hum Genet, vol. 23, no. 6, June 2015, pp. 854–62. Pubmed, doi:10.1038/ejhg.2014.189.
Singh A, Babyak MA, Nolan DK, Brummett BH, Jiang R, Siegler IC, Kraus WE, Shah SH, Williams RB, Hauser ER. Gene by stress genome-wide interaction analysis and path analysis identify EBF1 as a cardiovascular and metabolic risk gene. Eur J Hum Genet. 2015 Jun;23(6):854–862.

Published In

Eur J Hum Genet

DOI

EISSN

1476-5438

Publication Date

June 2015

Volume

23

Issue

6

Start / End Page

854 / 862

Location

England

Related Subject Headings

  • Trans-Activators
  • Socioeconomic Factors
  • Polymorphism, Single Nucleotide
  • Obesity
  • Metabolic Syndrome
  • Humans
  • Genome-Wide Association Study
  • Genetics & Heredity
  • Gene-Environment Interaction
  • Endophenotypes